Department of Pediatrics, Stanford University, Stanford, CA, USA.
Department of Bioengineering, Stanford University, Stanford, CA, USA.
Biomech Model Mechanobiol. 2019 Jun;18(3):779-796. doi: 10.1007/s10237-018-01114-0. Epub 2019 Jan 12.
Pulmonary arterial hypertension (PAH) is characterized by pulmonary vascular remodeling resulting in right ventricular (RV) dysfunction and ultimately RV failure. Mechanical stimuli acting on the vessel walls of the full pulmonary tree have not previously been comprehensively characterized. The goal of this study is to characterize wall shear stress (WSS) and strain in pediatric PAH patients at different stages of disease severity using computational patient-specific modeling. Computed tomography, magnetic resonance imaging and right heart catheterization data were collected and assimilated into pulmonary artery (PA) models for patients with and without PAH. Patients were grouped in three disease severity groups (control, moderate and severe) based on clinical evaluations. A finite element solver was employed to quantify hemodynamics and wall strains. To estimate WSS in the distal small PAs with diameters ranging from 50 to 500 [Formula: see text], a morphometric tree model was created, with inputs coming from outlets of the 3D model. WSS in the proximal PAs decreased with disease severity (control 20.5 vs. moderate 15.8 vs. severe 6.3 [Formula: see text], [Formula: see text]). Oscillatory shear index increased in the main pulmonary artery (MPA) with disease severity (0.13 vs. 0.13 vs. 0.2, [Formula: see text]). Wall strains measured by the first invariant of Green strain tensor decreased with disease severity (0.16 vs. 0.12 vs. 0.11, [Formula: see text]). Mean WSS for the distal PAs between 100 and 500 [Formula: see text] significantly increased with disease severity (20 vs. 52 vs. 116 [Formula: see text], [Formula: see text]). In conclusion, 3D flow simulations showed that WSS is significantly decreased in the MPA with disease while the mathematical morphometric model suggested increased WSS in the distal small vessels. Computational models can reveal mechanical stimuli acting on vessel walls that may inform patient risk stratification and flow shear experiments.
肺动脉高压(PAH)的特征是肺血管重构导致右心室(RV)功能障碍,最终导致 RV 衰竭。以前没有全面描述过作用于整个肺树血管壁的机械刺激。本研究的目的是使用计算患者特异性模型来描述不同疾病严重程度的儿科 PAH 患者的壁切应力(WSS)和应变。收集并整合了 CT、MRI 和右心导管检查数据,以建立有和没有 PAH 的患者的肺动脉(PA)模型。根据临床评估,患者被分为三组疾病严重程度(对照组、中度组和重度组)。有限元求解器用于量化血液动力学和壁应变。为了估计直径在 50 到 500μm 之间的远端小 PA 中的 WSS,创建了一个形态计量树模型,其输入来自 3D 模型的出口。随着疾病严重程度的增加,近端 PA 中的 WSS 降低(对照组为 20.5,中度组为 15.8,重度组为 6.3[Formula: see text])。主要肺动脉(MPA)中的振荡剪切指数随着疾病严重程度的增加而增加(0.13 比 0.13 比 0.2,[Formula: see text])。通过 Green 应变张量的第一不变量测量的壁应变随着疾病严重程度的降低而降低(0.16 比 0.12 比 0.11,[Formula: see text])。100 到 500μm 之间的远端 PA 的平均 WSS 随着疾病严重程度的增加而显著增加(20 比 52 比 116[Formula: see text],[Formula: see text])。总之,3D 流模拟显示,随着疾病的发展,MPA 中的 WSS 显著降低,而数学形态计量模型表明,远端小血管中的 WSS 增加。计算模型可以揭示作用于血管壁的机械刺激,这可能为患者风险分层和血流剪切实验提供信息。